Effect of changes in sodium or water intake on glomerular B2-kinin-binding sites.

In a previous study, we characterized a B2-kinin-binding site in rat glomerular membranes. We have now investigated the density and affinity of this binding site for bradykinin (BK) in rat glomerular membranes, in relation to the renal and urinary levels of kallikrein during changes in sodium and water intake. The density of BK-binding sites was reduced after 28 days of low-sodium diet (12.5 +/- 1.3 vs. control: 32.1 +/- 5.2 fmol/mg protein, P less than 0.05), whereas the concentration and activity of kallikrein was increased in the renal tissue and in the urine. Water deprivation for 4 days also resulted in a decreased density of binding sites (13.2 +/- 1.2 vs. control 32.1 +/- 5.2 fmol/mg protein, P less than 0.05) and, interestingly, renal kallikrein levels increased. During high salt consumption, urinary kallikrein activity increased but the renal concentration and activity of kallikrein was unchanged. In this high-sodium-loaded group, BK-binding site density was similar to controls receiving a normal-sodium diet (41.6 +/- 8.4 vs. control 32.1 +/- 5.2 fmol/mg protein). On the other hand, the binding affinity of BK did not change significantly in all experimental groups, and the binding specificity was not altered as BK remained the most potent agonist. Sodium depletion and water deprivation led to the same effects on BK-binding sites and on renal kallikrein. The renal glomerular BK-binding site density decreased in both conditions, whereas the renal level of kallikrein was enhanced. An inverse relationship between renal kinin levels and the density of glomerular BK-binding sites is therefore suggested.